Husain Kazim, Ansari Rais A, Ferder Leon
Kazim Husain, Leon Ferder, Department of Physiology, Pharmacology and Toxicology, Ponce School of Medicine and Health Sciences, Ponce, PR 00732, United States.
World J Cardiol. 2014 May 26;6(5):245-52. doi: 10.4330/wjc.v6.i5.245.
Epidemiological, preclinical and clinical studies established the association between high alcohol consumption and hypertension. However the mechanism through which alcohol raises blood pressure remains elusive. Several possible mechanisms have been proposed such as an imbalance of the central nervous system, impairment of the baroreceptors, enhanced sympathetic activity, stimulation of the renin-angiotensin-aldosterone system, increased cortisol levels, increased vascular reactivity due to increase in intracellular calcium levels, stimulation of the endothelium to release vasoconstrictors and loss of relaxation due to inflammation and oxidative injury of the endothelium leading to inhibition of endothelium-dependent nitric oxide production. Loss of relaxation due to inflammation and oxidative injury of the endothelium by angiotensin II leading to inhibition of endothelium-dependent nitric oxide production is the major contributors of the alcohol-induced hypertension. For the prevention of alcohol-induced hypertension is to reduce the amount of alcohol intake. Physical conditioning/exercise training is one of the most important strategies to prevent/treat chronic alcohol-induced hypertension on physiological basis. The efficacious pharmacologic treatment includes the angiotensin-converting enzyme (ACE) inhibitors or angiotensin II type 1 receptor blockers (ARBs) which have antioxidant activity and calcium channel blockers. The most effective prevention and treatment of alcohol-induced hypertension is physical exercise and the use of ACE inhibitors or ARBs in the clinic.
流行病学、临床前和临床研究证实了高酒精摄入量与高血压之间的关联。然而,酒精升高血压的机制仍不清楚。已经提出了几种可能的机制,如中枢神经系统失衡、压力感受器受损、交感神经活动增强、肾素-血管紧张素-醛固酮系统受刺激、皮质醇水平升高、细胞内钙水平升高导致血管反应性增加、刺激内皮细胞释放血管收缩剂以及由于内皮细胞的炎症和氧化损伤导致舒张功能丧失,进而抑制内皮依赖性一氧化氮生成。血管紧张素II导致内皮细胞炎症和氧化损伤,进而抑制内皮依赖性一氧化氮生成,导致舒张功能丧失,这是酒精性高血压的主要原因。预防酒精性高血压的方法是减少酒精摄入量。体育锻炼/运动训练是基于生理基础预防/治疗慢性酒精性高血压的最重要策略之一。有效的药物治疗包括具有抗氧化活性的血管紧张素转换酶(ACE)抑制剂或1型血管紧张素II受体阻滞剂(ARB)以及钙通道阻滞剂。临床上预防和治疗酒精性高血压最有效的方法是体育锻炼以及使用ACE抑制剂或ARB。